BMC Molecular and Cell Biology最新文献

{"title":"ALIX and ITCH localize to the base of primary cilia and negatively regulate ciliary Polycystin-2 levels.","authors":"Christina Rahlff Berggreen, Julie Laplace, Fabiola Campestre, Anna-Louise With Petersen, Anna Maria Fixdahl, Benjamin Mary, Saba Ghazanfar, Geyi Li, Lotta Elisabeth Wagner, Csenge K Rezi, Mohamed Chamlali, Zeinab Anvarian, Søren T Christensen, Helen L May-Simera, Lotte B Pedersen","doi":"10.1186/s12860-026-00571-1","DOIUrl":"10.1186/s12860-026-00571-1","url":null,"abstract":"<p><p>Primary cilia are antenna-like organelles that function as cellular hubs for signaling pathways, including Sonic hedgehog and signaling mediated by the Polycystin-1/Polycystin-2 cation channel complex. Proper regulation of signaling output depends on the dynamic control of ciliary protein composition, which involves intraflagellar transport-mediated trafficking, protein retrieval, and the shedding of extracellular vesicles from cilia. Here we identify ALIX, a protein previously linked to the biogenesis of small extracellular vesicles, as a novel component localized at the base of primary cilia in cultured mammalian cells. We show that ALIX retention at this site requires the ciliary kinesin-3 motor protein KIF13B, which physically interacts with ALIX and the E3 ubiquitin ligase ITCH. In turn, ITCH is enriched at the ciliary base and is essential for ALIX stability. Depletion of either ALIX or ITCH results in elevated ciliary levels of Polycystin-2, while ITCH loss additionally leads to constitutive accumulation of Smoothened, a key Sonic hedgehog effector, within the cilium. Collectively, our findings establish ALIX and ITCH as critical regulators of ciliary membrane protein homeostasis and signaling, acting in coordination with KIF13B to maintain proper ciliary function.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13041057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147302134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATP-related purinergic signaling via P2Y12 contributes to airway epithelial barrier integrity.","authors":"Kota Tsuya, Shuichiro Maruoka, Shinichi Okamoto, Sotaro Shikano, Mari Ujike, Shiho Yamada, Yusuke Kurosawa, Kenji Mizumura, Yutaka Kozu, Yasuhiro Gon","doi":"10.1186/s12860-026-00578-8","DOIUrl":"10.1186/s12860-026-00578-8","url":null,"abstract":"<p><p>BACKGROUND: The airway epithelial barrier, which defends against external pathogens, is compromised in bronchial asthma. This study investigated the roles of adenosine triphosphate (ATP) and specific purinergic receptors in airway epithelial barrier function. Using the 16HBE14o- human airway epithelial cell line, we measured barrier integrity using transepithelial electrical resistance and the apparent paracellular permeability coefficient. RESULTS: ATP enhanced barrier integrity in a dose-dependent manner without affecting cell proliferation. Real-time PCR revealed an increased expression of tight and adherens junction proteins, including E-cadherin and occludin, following ATP stimulation. Our findings suggest that P2Y12 contributes to ATP-related purinergic signaling associated with enhanced airway epithelial barrier integrity. CONCLUSIONS: These findings suggest that ATP-related purinergic signaling via P2Y12 may contribute to the regulation of airway epithelial barrier integrity in vitro. Further studies in more physiologically relevant systems are warranted to determine the clinical relevance of these observations. </p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13041268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147302143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin signaling engages divergent transcriptional mechanisms in neural and metabolic tissues.","authors":"Roshni Jain, Rutuj Kolhe, Cassandra Hui, Juli Petereit, Dennis Mathew","doi":"10.1186/s12860-026-00577-9","DOIUrl":"10.1186/s12860-026-00577-9","url":null,"abstract":"<p><p>BACKGROUND: Insulin signaling is a conserved regulator of growth, metabolism, and lifespan across metazoans. While its systemic roles are well established, the mechanisms by which insulin coordinates tissue-specific transcriptional programs that underlie distinct functional demands remain incompletely understood. In particular, the differential impact of reduced insulin signaling on different tissues has not been systematically explored. RESULTS: We performed a comparative transcriptomic analysis of Drosophila melanogaster olfactory sensory neurons (OSNs) and fat body (Fb) to investigate how reduced insulin signaling remodels gene expression in neural and metabolic tissues. Across both tissue types, insulin reduction suppressed key pathways involved in protein synthesis and mRNA surveillance, indicating shared regulatory responses. However, distinct tissue-specific transcriptional adaptations were also observed. In OSNs, insulin reduction led to the upregulation of synaptic and signaling genes, alongside the downregulation of proteostasis-related factors, suggesting enhanced neural plasticity that may come at the cost of long-term neuronal maintenance. In contrast, the Fb exhibited widespread metabolic suppression accompanied by feedback activation of stress-responsive insulin-like peptide genes, consistent with a shift toward hypometabolic adaptation. Network and pathway analyses revealed that these tissue-specific responses involved distinct regulatory architectures affecting core insulin pathway components and gene families. CONCLUSIONS: Our findings demonstrate that reduced insulin signaling elicits both shared and divergent transcriptional programs in neural and metabolic tissues of Drosophila melanogaster. These findings reveal how insulin signaling orchestrates tissue-specific transcriptional landscapes that may underlie differential resilience or vulnerability to cognitive and metabolic decline. </p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13019849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A nanobody-based degron system for targeted protein knockdown in Dictyostelium discoideum.","authors":"Hidenori Hashimura, Shoko Fujishiro, Nao Shimada, Tomoko Adachi, Toyoko Sugita, Satoshi Kuwana, Satoshi Sawai","doi":"10.1186/s12860-026-00572-0","DOIUrl":"10.1186/s12860-026-00572-0","url":null,"abstract":"<p><strong>Backgrounds: </strong>The cellular slime mold Dictyostelium discoideum is a widely used model system for studying basic processes in cell and developmental biology. While genetic tools, such as targeted gene disruption by homologous recombination and genome editing using CRISPR/Cas9, are well-established in D. discoideum, efficient methods for conditional loss-of-function studies are limited. Here, we developed a nanobody-based degron system for D. discoideum based on ALFA-tagged protein recruitment to the Skp1-Cullin-F-box (SCF) complex.</p><p><strong>Results: </strong>ALFA-tagged Histone H1 was efficiently degraded by expressing anti-ALFA nanobody (NbALFA) fused to the D. discoideum FbxD F-box domain ('dictyGrad-ALFA'). Cell type-specific targeting was achieved by expressing dictyGrad-ALFA under prestalk- and prespore-specific gene promoters. Furthermore, targeting of adenylyl cyclase A (ACA) resulted in the expected aggregation-deficient phenotype, validating the efficacy of dictyGrad-ALFA-mediated protein depletion. Cell type-specific ACA degradation delayed development but eventually resulted in normal fruiting bodies. Our ALFA-tag approach was further used for conditional knockdown in combination with the auxin-inducible degron 2 (AID2) system, which relies on indole-3-acetic acid (IAA)-dependent binding between NbALFA-mAID and a OsTIR-F-box-Skp1A fusion protein. We obtained efficient IAA-induced degradation in prestalk cells; however, efficiency was low in other cell types.</p><p><strong>Conclusions: </strong>Together, these systems pave the way for conditional and cell type-specific protein degradation in D. discoideum, enabling functional analyses of genes essential for growth and development.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13020093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human urine-derived stem exosomes inhibit inflammation and oxidative stress in sepsis-related acute kidney injury.","authors":"Lulu Liu, Lili Ding, Zhaorui Sun, Weichao Ding, Haijun Sun, Maohong Xia, Quan Li","doi":"10.1186/s12860-026-00575-x","DOIUrl":"10.1186/s12860-026-00575-x","url":null,"abstract":"<p><strong>Objective: </strong>The objective of this study was to explore the mechanisms by which urine - derived stem cell exosomes (USCexo) alleviate sepsis - related acute kidney injury (SAKI), as acute kidney injury often complicates sepsis with unclear role of USCexo in SAKI while stem cell exosomes show potential in AKI treatment.</p><p><strong>Methods: </strong>Human urine - derived stem cells (USCs) were isolated from human urine and characterized via flow cytometry. A sepsis - related acute kidney injury mouse model was induced by cecal ligation and puncture (CLP). The mice were divided into a control group receiving phosphate - buffered saline (PBS) and an experimental group receiving USCexo via tail vein injection. Survival rate, renal damage evaluated by HE staining, and renal function assessed by sCr and BUN levels were measured. Renal RNA was extracted to analyze apoptosis and oxidative stress. In vitro, qRT - PCR was used to assess the inflammatory response in macrophages treated with USCexo.</p><p><strong>Results: </strong>Treatment with USC - derived exosomes led to a reduction in the levels of pathological injury, sCr, and BUN. It inhibited renal cell apoptosis and oxidative stress, decreased the infiltration of inflammatory cells, and protected renal function in SAKI mice. Additionally, USCexo suppressed the inflammatory response of primary peritoneal macrophages induced by lipopolysaccharide (LPS).</p><p><strong>Conclusions: </strong>USC - derived exosomes protect against SAKI by inhibiting oxidative stress and inflammation, which provides a theoretical basis for the potential use of USCexo in the treatment of SAKI.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13014871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of prey quality through the life cycle of the social amoeba Dictyostelium discoideum.","authors":"Heng Liang, Margaret I Steele, Kaifeng Hu, Steven M Wolf, David C Queller, Joan E Strassmann","doi":"10.1186/s12860-026-00574-y","DOIUrl":"10.1186/s12860-026-00574-y","url":null,"abstract":"<p><p>BACKGROUND: Generalist consumers can eat a variety of foods, but they are not necessarily equally beneficial. Different feeding histories can influence the fitness of genetically similar individuals. Dictyostelium discoideum is a unicellular generalist predator amoeba that eats bacteria. When bacteria are depleted, amoebae enter the social cycle and aggregate to form a fruiting body, in which about a fifth of the amoebae die to form a stalk while the rest form spores at the top of the stalk. RESULTS: In this study, we examined the fitness of D. discoideum when grown on three bacterial prey types: poorly palatable wild-type Pseudomonas vindicans, a more palatable mutant of the same species, and the high-quality food bacterium Klebsiella pneumoniae. We used these three bacteria to examine how feeding history shapes fitness throughout the life cycle by measuring proliferation of amoebae, then following spores through germination, plaque formation, and plaque expansion. Amoebae grew on unpalatable P. vindicans only when seeded at high density, and even then, proliferated more slowly. When amoebae with different feeding histories were mixed and allowed to form chimeric fruiting bodies, those cells fed on palatable versus unpalatable P. vindicans did not differ significantly in their spore contribution, except when under an additional stress of the translational inhibitor G418, which makes cells that previously fed on unpalatable P. vindicans contribute fewer cells in spores. Oddly, the amoebae that fed on the good food bacterium Klebsiella pneumoniae contributed fewer spores when mixed with cells that fed on either of the P. vindicans clones. Surprisingly, though feeding on unpalatable prey was not a hindrance in the social stage, downstream effects were observed. Spores produced on either P. vindicans strain germinated more slowly than those made from amoebae fed on Klebsiella pneumoniae. CONCLUSIONS: Low prey quality strongly affects D. discoideum fitness during the vegetative stage but does not generally lower social competitive ability. Nevertheless, it does affect fitness after the social cycle by reducing the hatching rate of spores. </p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13011474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146206676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose-dependent effects of atorvastatin on inflammatory response in endothelial cells: MMP/TIMP balance and in vitro wound closure assay.","authors":"Betül İşiner, Aslı Fahriye Ceylan, Büşra Görgün, Leyla Didem Kozacı","doi":"10.1186/s12860-026-00573-z","DOIUrl":"10.1186/s12860-026-00573-z","url":null,"abstract":"<p><strong>Background: </strong>Clinical and preclinical evidence suggests that inflammation is closely associated with various arterial diseases. Multiple studies have reported the effects of statins on different cell types, yet the effects of atorvastatin (ATV) and its mechanisms on inflamed HUVECs' cellular responses are still under investigation. This study investigates how different doses of ATV affect inflammatory responses, extracellular matrix (ECM) regulators, and cell migration capacity assessed by an in vitro scratch wound closure assay in lipopolysaccharide (LPS) stimulated endothelial cells.</p><p><strong>Methods: </strong>ATV was applied to cells at different doses (5-10-50 µM) with or without LPS (20 ng/mL). Cell proliferation and toxicity were investigated in the indicated groups. Then, the possible effects of ATV on MMP-2, MMP-9, TIMP-1,TIMP-2 expression levels, scratch-closure (cell migration) time were examined. Gene expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 was quantified by qPCR, while protein levels were determined by Western blotting. Cell migration was evaluated using a scratch assay and real-time imaging system.</p><p><strong>Results: </strong>High-dose ATV was more cytotoxic, while wound closure times showed a numerical increase that did not reach statistical significance under LPS stimulation. While low-dose ATV increased MMP and TIMP expressions, high-dose treatment reduced TIMP-1 and disturbed the MMP/TIMP balance. This imbalance was accompanied by reduced cellular recovery capacity under inflammatory stress.</p><p><strong>Conclusions: </strong>This study highlights the complex cellular effects of ATV under inflammatory conditions, supporting its context- and dose-dependent role in endothelial cell behavior and matrix regulation. These findings highlight the importance of dosage optimization in therapeutic contexts targeting vascular inflammation and provide novel insight into how statin dosing influences endothelial recovery mechanisms, beyond cholesterol regulation.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13011320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146206687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic suppressor of autophagy defects in huntingtin null cells identified using a mutagenesis screen in Dictyostelium discoideum.","authors":"Lauren Cuoco, Shelbi E Gill, Luc Francois, Sarah Souders, Caroline DeMasi, Jeffrey R Moore, Frédéric J J Chain","doi":"10.1186/s12860-026-00570-2","DOIUrl":"10.1186/s12860-026-00570-2","url":null,"abstract":"<p><strong>Background: </strong>Huntingtin (HTT) is an important gene for cellular processes such as autophagy, and its loss leads to neurodegenerative disease phenotypes. In Dictyostelium discoideum, HTT-null (htt-) cells exhibit impaired basal autophagy and fail to develop in the presence of ammonium chloride.</p><p><strong>Results: </strong>Here we conducted a mutagenesis screen on htt- cells to identify potential genetic suppressors of the htt- phenotype. A mutant strain was isolated that counteracts many of the hallmark defects engendered with htt loss. This mutant, htt-;supX, rescues the growth, cargo degradation defects, developmental timing, and autophagic flux of htt- cells under ammonium chloride stress, representing a partial rescue of the htt- phenotype. Whole-genome sequencing revealed four mutations in the mutant strain affecting genes involved in vesicle trafficking, signal transduction, metal ion regulation, and fatty acid elongation. Transcriptome sequencing further identified 208 differentially expressed genes in the mutant strain, including genes whose expression was returned to wild-type levels, suggesting a potential mechanism by which htt-;supX mediates phenotypic recovery. Among these, five genes have known autophagy-related functions and may be implicated in pathways such as Rab GTPase regulation and SNARE-mediated vesicle fusion.</p><p><strong>Conclusions: </strong>Our study highlights the ability of second-site mutations to restore autophagic function in the absence of HTT and identifies candidate genes and pathways for further investigation into Huntington's Disease models and autophagy modulation.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Wnt/β-catenin pathway maintains homeostasis of amniocytes in Down syndrome.","authors":"Xiaoying Chen, Miaochun Lin, Shan Chen, Zhengsen Wang, Zhaohui Li, Juan Zuo","doi":"10.1186/s12860-026-00569-9","DOIUrl":"10.1186/s12860-026-00569-9","url":null,"abstract":"<p><p>BACKGROUND: Down syndrome (DS), which is caused by partial or complete triplication of chromosome 21, may cause a range of clinical features. Although most fetuses with DS exhibit typical characteristics, the molecular pathogenesis underlying DS remains unclear. Wnt signaling is known to play a crucial role in fetal growth and development. However, the link between Wnt signaling and the abnormal development of fetuses with DS remains poorly understood. In this study, our objective was to investigate the dysregulation of the Wnt/β-catenin pathway in the amniocytes of fetuses diagnosed with DS. To this end, we obtained amniocytes from 10 fetuses diagnosed with DS and determined the expression levels of key proteins activated by the Wnt/β-catenin pathway, oxidative stress, cell proliferation, and apoptosis in these amniocytes using western blot and cellular immunofluorescence methods. Subsequently, components of the Wnt/β-catenin pathway were upregulated in amniocytes from fetuses diagnosed with DS and expression of related proteins was detected. The differences were evaluated using Student’s t-test or analysis of variance, followed by Tukey’s test. RESULTS: We found that the Wnt/β-catenin pathway was inhibited in DS fetal amniocytes compared to normal fetal amniocytes, and cell proliferation was reduced, along with increased oxidative stress and apoptosis. In contrast, up-regulation of the Wnt/β-catenin pathway in DS amniocytes increased cell proliferation, decreased oxidative stress and apoptosis, and ultimately improved cell growth. CONCLUSIONS: The Wnt/β-catenin pathway mitigates excessive apoptosis caused by oxidative stress, promotes cellular proliferation, and maintains homeostasis in DS amniocytes. These findings reveal a novel molecular mechanism underlying the abnormal regulation of the Wnt/β-catenin pathway during the development of fetuses with DS, thereby suggesting potential targeted therapies for DS. </p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12947344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolation and characterization of mesenchymal stem cells from nasal polyps and olfactory mucosa: a comparative analysis of proliferation and multi-lineage differentiation capacity.","authors":"Negin Khosravi, Zahra Pourmohammadi-Bejarpasi, Mehryar Habibi Roudkenar, Samin Abed, Ehsan Kazemnezhad Leyli, Shadman Nemati","doi":"10.1186/s12860-026-00564-0","DOIUrl":"10.1186/s12860-026-00564-0","url":null,"abstract":"<p><p>BACKGROUND: Nasal polyps (NPs) and olfactory mucosa (OM) are emerging as potential sources of mesenchymal stem cells (MSCs), which hold promise for regenerative medicine due to their multipotent differentiation capabilities. This study aimed to isolate MSCs from nasal polyps (NP-MSCs) and evaluate their differentiation potentials in comparison with healthy olfactory mucosa (OM-MSCs). METHODS: 16 human samples from NP and OM tissues were studied and MSCs were isolated enzymatically. Flow-cytometry analysis was done to characterize the isolated cells; then, tri-lineage differentiation capacity of SCs into osteoblasts, adipocytes, and neurons was evaluated using the differentiation mediums. Finally, the proliferation rate was assessed by Cell Counting Kit-8. RESULTS: The outgrowth of cells from NP tissue was observed approximately three days earlier than that from OM tissue. OM-MSCs and NP‐MSCs showed expression of CD markers of mesenchymal cells, including CD105, CD73, CD90, and CD44, but not the markers of hematopoietic cells including CD14, CD45, CD34, and HLA-DR. Cell viability and proliferation rates of NP‐MSCs and OM‐MSCs were both high, and significantly higher in OM-MSC (p-value < 0.001). The multi-lineage differentiation (osteogenic, adipogenic, and neurogenic) of OM-MSCs and NP-MSCs was confirmed. CONCLUSION: These results showed that MSCs are present in NPs with noticeable differentiation potentials. These cells may play some roles in the pathogenesis of NP. Additionally, nasal polyps, as biowastes, represent a potential novel source of MSCs. </p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}